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Cardiovascular System > 14. Haemostasis 2 > Flashcards

14. Haemostasis 2 Flashcards

1
Q

Normal haemostasis

A

Balance between fibrinolytic factors and anticoagulant proteins + coagulation factors and platelets

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2
Q

What causes bleeding disorders?

A

Too little pro-coagulant factors (VIII,IX,XI)

Too many anticoagulant factors

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3
Q

List 4 characteristics of abnormal bleeding

A

‘Spontaneous’
Out of proportion to the trauma/injury
Unduly prolonged
Restarts after appearing to stop

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4
Q

What clinical feature is common to all bleeding disorders?

A

Easy bruising

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5
Q

Give 3 examples of significant bleeds

A

Nosebleed not stopped by 10 mins compression
Cutaneous haemorrhage
Prolonged (>15 mins) bleeding from trivial wounds

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6
Q

List 3 defects of primary haemostasis

A

Deficiency or defective:
Collagen (steroid therapy, age, scurvy)
Von Willebrand factor (genetic disease)
Platelets (aspirin, thrombocytopenia)

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7
Q

What happens to patients with Von Willebrand factor deficiency?

A

Damaged vessel wall
But no VWF, so platelets can’t stick (as move too fast)
Patient bleeds as can’t form primary haemostatic plug
(bleed from outset)

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8
Q

Describe the pattern of bleeding of a defect in primary haemostasis.

A 
Immediate
Easy bruising
Nosebleeds (prolonged: >20 mins)
Gum bleeding (prolonged)
Menorrhagia (anaemia)
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9
Q

What is a characteristic feature of thrombocytopenia?

A

Petechiae (bleeding spots)

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10
Q

What is the main role of primary haemostasis?

A

Formation of an unstable platelet plug
(through platelet adhesion and aggregation)
Limits blood loss and provides surface for coagulation

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11
Q

What is the main role of secondary haemostasis?

A

Stabilisation of the platelet plug with fibrin
Blood coagulation
Stops blood loss

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12
Q

Why is there a lag between the administration of a tissue factor trigger and the thrombin burst?

A

This is when cofactors and clotting factors are synthesised.

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13
Q

Describe the cause of haemophilia A

A

There is insufficient FVIII
Thrombin generation “boost” doesn’t happen
Failure of thrombin generation
Failure to generate fibrin mesh to stabilise platelet plug

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14
Q

Attempted haemostasis in haemophilia A

A

Primary haemostatic plug forms so initially stop bleeding, but it doesn’t get stabilised so falls apart

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15
Q

Defects of secondary haemostasis

A

Deficiency or defect of coagulation factors

Poor thrombin burst, poor fibrin mesh

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16
Q

Genetic defects of secondary haemostasis

A

Haemophilia: FVIII or FIX deficiency

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17
Q

List 4 acquired disorders of secondary haemostasis

A

Liver disease (most coagulation factors are made in the liver)
Drugs (warfarin: inhibits synthesis, others block function)
Dilution (results from volume replacement: when not enough plasma is replaced)
Consumption (DIC)

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18
Q

What is DIC an abbreviation for? What is DIC?

A

Disseminated intravascular coagulation
Generalised activation of the coagulation- expression of tissue factor inside vasculature
Consumes and depletes clotting factors and platelets
Activates fibrinolysis- depletes fibrinogen

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19
Q

What is DIC associated with?

A

Sepsis
Major tissue damage
Inflammation

20
Q

What are the consequences of DIC?

A

Widespread bleeding

Deposition of fibrin in vessels causes organ failure

21
Q

Describe the pattern of bleeding of defects in secondary haemostasis.

A 
Delayed (after primary haemostasis)
Prolonged
Bleed deeper into joints and muscles. 
Not from small cuts (primary haemostasis is fine)
Nosebleeds rare
Bleeding after trauma/ surgery 
Easy bruising
22
Q

What is the hallmark of haemophilia?

A

Haemarthrosis: bleeding into joints

23
Q

Defects in fibrinolysis prevalence

A

Not so common

24
Q

What will excess fibrinolytic activity cause?

A

Excess bleeding

25
Q

State 2 defects of clot stability

A 
Excess fibrinolytic (plasmin, tPA)
Deficient antifibrinolytic (antiplasmin)
26
Q

What causes excess fibrinolytic activity (plasmin, TPA)?

A 
Therapeutic administration (given to people with strokes to break down blood clot)
Some tumours
27
Q

What causes deficient antifibrinolytic activity (antiplasmin))?

A

Antiplasmin deficiency (genetic)

28
Q

What causes anticoagulant excess?

A

Usually therapeutic administration e.g. Heparin (which activates antithrombin)

29
Q

Describe the characteristics of thrombosis

A 
Excess FVIII
Increased procoagulant activity
Deficient anticoagulant activity
Blood clot should not have been formed, unnecessary, not preceded by bleeding 
Blood vessel intact with clot inside it
Pathological clot formation
30
Q

What are the effects of thrombosis?

A

Obstructed flow of blood

Embolism (migration of the thrombus)

31
Q

What may obstructed flow in an artery or vein cause?

A

Artery: stops blood flow to organ/ area of tissue, usually more immediately serious e.g. MI, stroke, limb ischaemia
Vein: blood can usually still return to heart via a different route. May cause pain/ swelling

32
Q

What may arterial emboli cause?

A

Stroke

Limb ischaemia

33
Q

What may venous emboli cause?

A 
Pulmonary embolism
(shortness of breath, chest pain, sudden death)
34
Q

Deep vein thrombosis

A

Venous return of blood obstructed

painful, swollen leg

35
Q

How does risk of thrombosis change with age?

A

Increases

36
Q

What are the 4 consequences of thromboembolism?

A

Death
Recurrence
Thrombophlebitic syndrome
Pulmonary hypertension

37
Q

List 3 possible contributory factors to thrombosis

A

Genetics
Acute stimulus
Effect of age, illness, medication

38
Q

What are the 3 components of Virchow’s triad?

A 
Blood hypercoagulability (dominant in venous thrombosis)
Vessel wall injury (dominant in arterial thrombosis)
Stasis (contributes to both)
39
Q

Increased risk of Venous thrombosis: Blood

A

Deficiency of anticoagulant proteins e.g. Antithrombin

Increased coagulant proteins e.g. FVIII

40
Q

Increased risk of Arterial thrombosis: vessel wall

A

Many proteins active in coagulation are expressed on the surface of endothelial cells e.g. Thrombomodulin
Expression is altered in inflammation e.g. infection

41
Q

Increased risk of thrombosis: Flow

A

Reduced flow (stasis) increases the risk of venous thrombosis e.g.: surgery, fracture

42
Q

What do people with Thrombophilia have an increased tendency of?

A

Increased tendency of thrombosis

43
Q

What are the signs of thrombophilia?

A

Thrombosis at young age
Idiopathic thrombosis
Multiple thromboses
Thrombosis whist anticoagulated

44
Q

Which 4 conditions will alter blood coagulation, vessel wall and/ or flow to precipitate thrombosis?

A

Pregnancy
Malignancy
Surgery
Inflammatory response

45
Q

What is lysing thrombi not often a method of treatment?

A

There is a high risk of bleeding

46
Q

What is the main approach to treating thrombi?

A

Limit recurrence/ extension/ emboli:
Increase anticoagulant activity e.g. heparin
Decrease procoagulant factors e.g. Warfarin
Inhibit procoagulant factors

Cardiovascular System (16 decks)

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